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Microbial Modulation in Inflammatory Bowel Diseases. 炎症性肠病中的微生物调节。
IF 6 4区 医学
Immune Network Pub Date : 2022-12-01 DOI: 10.4110/in.2022.22.e44
Jongwook Yu, Jae Hee Cheon
{"title":"Microbial Modulation in Inflammatory Bowel Diseases.","authors":"Jongwook Yu,&nbsp;Jae Hee Cheon","doi":"10.4110/in.2022.22.e44","DOIUrl":"https://doi.org/10.4110/in.2022.22.e44","url":null,"abstract":"<p><p>Gut dysbiosis is one of prominent features in inflammatory bowel diseases (IBDs) which are of an unknown etiology. Although the cause-and-effect relationship between IBD and gut dysbiosis remains to be elucidated, one area of research has focused on the management of IBD by modulating and correcting gut dysbiosis. The use of antibiotics, probiotics either with or without prebiotics, and fecal microbiota transplantation from healthy donors are representative methods for modulating the intestinal microbiota ecosystem. The gut microbiota is not a simple assembly of bacteria, fungi, and viruses, but a complex organ-like community system composed of numerous kinds of microorganisms. Thus, studies on specific changes in the gut microbiota depending on which treatment option is applied are very limited. Here, we review previous studies on microbial modulation as a therapeutic option for IBD and its significance in the pathogenesis of IBD.</p>","PeriodicalId":13307,"journal":{"name":"Immune Network","volume":"22 6","pages":"e44"},"PeriodicalIF":6.0,"publicationDate":"2022-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/8f/cf/in-22-e44.PMC9807960.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10518552","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Context-Dependent Regulation of Type17 Immunity by Microbiota at the Intestinal Barrier. 肠道屏障微生物群对 17 型免疫的情境依赖性调控
IF 4.3 4区 医学
Immune Network Pub Date : 2022-09-26 eCollection Date: 2022-12-01 DOI: 10.4110/in.2022.22.e46
Begum Akuzum, June-Yong Lee
{"title":"Context-Dependent Regulation of Type17 Immunity by Microbiota at the Intestinal Barrier.","authors":"Begum Akuzum, June-Yong Lee","doi":"10.4110/in.2022.22.e46","DOIUrl":"10.4110/in.2022.22.e46","url":null,"abstract":"<p><p>T-helper-17 (Th17) cells and related IL-17-producing (type17) lymphocytes are abundant at the epithelial barrier. In response to bacterial and fungal infection, the signature cytokines IL-17A/F and IL-22 mediate the antimicrobial immune response and contribute to wound healing of injured tissues. Despite their protective function, type17 lymphocytes are also responsible for various chronic inflammatory disorders, including inflammatory bowel disease (IBD) and colitis associated cancer (CAC). A deeper understanding of type17 regulatory mechanisms could ultimately lead to the discovery of therapeutic strategies for the treatment of chronic inflammatory disorders and the prevention of cancer. In this review, we discuss the current understanding of the development and function of type17 immune cells at the intestinal barrier, focusing on the impact of microbiota-immune interactions on intestinal barrier homeostasis and disease etiology.</p>","PeriodicalId":13307,"journal":{"name":"Immune Network","volume":"22 6","pages":"e46"},"PeriodicalIF":4.3,"publicationDate":"2022-09-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/86/ae/in-22-e46.PMC9807962.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10518547","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Engineering Cell Therapies for Autoimmune Diseases: From Preclinical to Clinical Proof of Concept. 治疗自身免疫性疾病的工程细胞疗法:从临床前到临床概念验证。
IF 4.3 4区 医学
Immune Network Pub Date : 2022-09-21 eCollection Date: 2022-10-01 DOI: 10.4110/in.2022.22.e37
Sangwook Oh, Aimee S Payne
{"title":"Engineering Cell Therapies for Autoimmune Diseases: From Preclinical to Clinical Proof of Concept.","authors":"Sangwook Oh, Aimee S Payne","doi":"10.4110/in.2022.22.e37","DOIUrl":"10.4110/in.2022.22.e37","url":null,"abstract":"<p><p>Autoimmune diseases are caused by a dysfunction of the acquired immune system. In a subset of autoimmune diseases, B cells escaping immune tolerance present autoantigen and produce cytokines and/or autoantibodies, resulting in systemic or organ-specific autoimmunity. Therefore, B cell depletion with monoclonal Abs targeting B cell lineage markers is standard care therapy for several B cell-mediated autoimmune disorders. In the last 5 years, genetically-engineered cellular immunotherapies targeting B cells have shown superior efficacy and long-term remission of B cell malignancies compared to historical clinical outcomes using B cell depletion with monoclonal Ab therapies. This has raised interest in understanding whether similar durable remission could be achieved with use of genetically-engineered cell therapies for autoimmunity. This review will focus on current human clinical trials using engineered cell therapies for B cell-associated autoimmune diseases.</p>","PeriodicalId":13307,"journal":{"name":"Immune Network","volume":"22 5","pages":"e37"},"PeriodicalIF":4.3,"publicationDate":"2022-09-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/e4/bd/in-22-e37.PMC9634148.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9666991","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Outstanding Features of COVID-19 Overlapping Primary Immunodeficiency in Children. COVID-19重叠儿童原发性免疫缺陷的突出特征
IF 6 4区 医学
Immune Network Pub Date : 2022-08-04 eCollection Date: 2022-08-01 DOI: 10.4110/in.2022.22.e30
Qi Jiang, Qian Yang, Man Man Niu, Peng Hu
{"title":"Outstanding Features of COVID-19 Overlapping Primary Immunodeficiency in Children.","authors":"Qi Jiang,&nbsp;Qian Yang,&nbsp;Man Man Niu,&nbsp;Peng Hu","doi":"10.4110/in.2022.22.e30","DOIUrl":"https://doi.org/10.4110/in.2022.22.e30","url":null,"abstract":"https://immunenetwork.org Coronavirus disease 2019 (COVID-19) caused by severe acute respiratory syndrome coronavirus 2, is a highly transmittable and contagious infection among the general population, especially in individuals with immune defects regardless of primary immunodeficiencies (PID) or secondary immunodeficiencies caused by infectious agents and drugs. PID, caused by genetic defects, is referred to the inability to produce a normal complement of Abs or immunologically sensitized T cells especially in response to specific Ags. Registry and survey data from a variety of sources reveal an incidence for all PID ranging from 1 in 10,000 to 1 in 2,000 live births. Individual PID may be rare, but altogether, they are exactly frequent. Admittedly, little is known, to date, about the clinical features of COVID-19 overlapping PID.","PeriodicalId":13307,"journal":{"name":"Immune Network","volume":"22 4","pages":"e30"},"PeriodicalIF":6.0,"publicationDate":"2022-08-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/e4/72/in-22-e30.PMC9433195.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"33454305","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 1
Why Should We Consider Potential Roles of Oral Bacteria in the Pathogenesis of Sjögren Syndrome? 为什么我们应该考虑口腔细菌在Sjögren综合征发病机制中的潜在作用?
IF 6 4区 医学
Immune Network Pub Date : 2022-08-03 eCollection Date: 2022-08-01 DOI: 10.4110/in.2022.22.e32
Sung-Ho Chang, Sung-Hwan Park, Mi-La Cho, Youngnim Choi
{"title":"Why Should We Consider Potential Roles of Oral Bacteria in the Pathogenesis of Sjögren Syndrome?","authors":"Sung-Ho Chang,&nbsp;Sung-Hwan Park,&nbsp;Mi-La Cho,&nbsp;Youngnim Choi","doi":"10.4110/in.2022.22.e32","DOIUrl":"https://doi.org/10.4110/in.2022.22.e32","url":null,"abstract":"<p><p>Sjögren syndrome (SS) is a chronic autoimmune disorder that primarily targets the salivary and lacrimal glands. The pathology of these exocrine glands is characterized by periductal focal lymphocytic infiltrates, and both T cell-mediated tissue injury and autoantibodies that interfere with the secretion process underlie glandular hypofunction. In addition to these adaptive mechanisms, multiple innate immune pathways are dysregulated, particularly in the salivary gland epithelium. Our understanding of the pathogenetic mechanisms of SS has substantially improved during the past decade. In contrast to viral infection, bacterial infection has never been considered in the pathogenesis of SS. In this review, oral dysbiosis associated with SS and evidence for bacterial infection of the salivary glands in SS were reviewed. In addition, the potential contributions of bacterial infection to innate activation of ductal epithelial cells, plasmacytoid dendritic cells, and B cells and to the breach of tolerance via bystander activation of autoreactive T cells and molecular mimicry were discussed. The added roles of bacteria may extend our understanding of the pathogenetic mechanisms and therapeutic approaches for this autoimmune exocrinopathy.</p>","PeriodicalId":13307,"journal":{"name":"Immune Network","volume":"22 4","pages":"e32"},"PeriodicalIF":6.0,"publicationDate":"2022-08-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/d6/a1/in-22-e32.PMC9433196.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"33454301","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 1
Omicron Subvariants, Including BA.4 and BA.5, Substantially Preserve T Cell Epitopes of Ancestral SARS-CoV-2. 包括BA.4和BA.5在内的组粒亚变体大量保留了祖先SARS-CoV-2的T细胞表位。
IF 6 4区 医学
Immune Network Pub Date : 2022-08-03 eCollection Date: 2022-08-01 DOI: 10.4110/in.2022.22.e29
Kyemyung Park, Seung Jin Choi, Eui-Cheol Shin
{"title":"Omicron Subvariants, Including BA.4 and BA.5, Substantially Preserve T Cell Epitopes of Ancestral SARS-CoV-2.","authors":"Kyemyung Park,&nbsp;Seung Jin Choi,&nbsp;Eui-Cheol Shin","doi":"10.4110/in.2022.22.e29","DOIUrl":"https://doi.org/10.4110/in.2022.22.e29","url":null,"abstract":"https://immunenetwork.org The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) Omicron variants (B.1.1.529 and related) that emerged in November 2021 have spread worldwide, and are designated a variant of concern by the World Health Organization (WHO) (1). They have become the dominant strains, comprising >99% of newly deposited SARS-CoV-2 sequences in GISIAD (www. gisaid.org) as of May 16, 2022 (2). Following the emergence of B.1.1.529 (BA.1), BA.2 (often called stealth Omicron) soon became the most prevalent sublineage worldwide. Subsequent subvariants, including BA.2.9, BA.2.12.1, BA.4, and BA.5, are now rapidly dominating the circulating Omicron subvariants in originating regions, and are beginning to spread globally (2). The dominance of Omicron variants and their rapid evolution into various subvariants have raised concerns regarding the effects of the immunity elicited by natural infection or vaccination. As evolution continues, the variants’ spike proteins exhibit higher affinities toward ACE2, and/ or increasing capacity for evading preformed neutralizing antibodies induced by previous natural infection or vaccination (3-5). These changes are consistent with increased breakthrough infections and re-infections with Omicron variants (6,7).","PeriodicalId":13307,"journal":{"name":"Immune Network","volume":"22 4","pages":"e29"},"PeriodicalIF":6.0,"publicationDate":"2022-08-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/9a/2e/in-22-e29.PMC9433189.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"33454304","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 6
As a Modulator, Multitasking Roles of SIRT1 in Respiratory Diseases. SIRT1在呼吸系统疾病中的多任务调节作用
IF 6 4区 医学
Immune Network Pub Date : 2022-06-20 eCollection Date: 2022-06-01 DOI: 10.4110/in.2022.22.e21
Yunxin Zhou, Fan Zhang, Junying Ding
{"title":"As a Modulator, Multitasking Roles of SIRT1 in Respiratory Diseases.","authors":"Yunxin Zhou,&nbsp;Fan Zhang,&nbsp;Junying Ding","doi":"10.4110/in.2022.22.e21","DOIUrl":"https://doi.org/10.4110/in.2022.22.e21","url":null,"abstract":"<p><p>As far the current severe coronavirus disease 2019 (COVID-19), respiratory disease is still the biggest threat to human health. In addition, infectious respiratory diseases are particularly prominent. In addition to killing and clearing the infection pathogen directly, regulating the immune responses against the pathogens is also an important therapeutic modality. Sirtuins belong to NAD+-dependent class III histone deacetylases. Among 7 types of sirtuins, silent information regulator type-1 (SIRT1) played a multitasking role in modulating a wide range of physiological processes, including oxidative stress, inflammation, cell apoptosis, autophagy, antibacterial and antiviral functions. It showed a critical effect in regulating immune responses by deacetylation modification, especially through high-mobility group box 1 (HMGB1), a core molecule regulating the immune system. SIRT1 was associated with many respiratory diseases, including COVID-19 infection, bacterial pneumonia, tuberculosis, and so on. Here, we reviewed the latest research progress regarding the effects of SIRT1 on immune system in respiratory diseases. First, the structure and catalytic characteristics of SIRT1 were introduced. Next, the roles of SIRT1, and the mechanisms underlying the immune regulatory effect through HMGB1, as well as the specific activators/inhibitors of SIRT1, were elaborated. Finally, the multitasking roles of SIRT1 in several respiratory diseases were discussed separately. Taken together, this review implied that SIRT1 could serve as a promising specific therapeutic target for the treatment of respiratory diseases.</p>","PeriodicalId":13307,"journal":{"name":"Immune Network","volume":"22 3","pages":"e21"},"PeriodicalIF":6.0,"publicationDate":"2022-06-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/05/35/in-22-e21.PMC9250864.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40569100","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 4
Comparison of Waning Immunity Between Booster Vaccination and 2-Dose Vaccination With BNT162b2. 加强接种与2次接种BNT162b2免疫减弱的比较。
IF 6 4区 医学
Immune Network Pub Date : 2022-06-17 eCollection Date: 2022-08-01 DOI: 10.4110/in.2022.22.e31
Jiwon Jung, Ji Yeun Kim, Ji-Soo Kwon, Sung-Cheol Yun, Sung-Han Kim
{"title":"Comparison of Waning Immunity Between Booster Vaccination and 2-Dose Vaccination With BNT162b2.","authors":"Jiwon Jung,&nbsp;Ji Yeun Kim,&nbsp;Ji-Soo Kwon,&nbsp;Sung-Cheol Yun,&nbsp;Sung-Han Kim","doi":"10.4110/in.2022.22.e31","DOIUrl":"https://doi.org/10.4110/in.2022.22.e31","url":null,"abstract":"S1 specific IgG Ab was measured using an in-house developed ELISA, and the data are presented in IU/ml. The interferon-gamma ELISPOT assay was used to assess the SARS-CoV-2-specific T cell response in isolated PBMCs. T cells were stimulated using SARS-CoV-2 spike-overlapping peptides (Miltenyi Biotec, Bergisch Gladbach, Germany), and the number of spot-forming cells per 5.0×10 5 PBMCs were counted with an automated ELISPOT reader (AID iSPOT; Autoimmun Diagnostika GmbH, Strassberg, Germany). A linear mixed regression model was used to compare the slope from the peak Ab titer to the lowest Ab titer (23 wk after the second vaccination) and the slope from the peak Ab titer","PeriodicalId":13307,"journal":{"name":"Immune Network","volume":"22 4","pages":"e31"},"PeriodicalIF":6.0,"publicationDate":"2022-06-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/06/bc/in-22-e31.PMC9433190.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"33454300","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 2
Tobacco Smoking Could Accentuate Epithelial-Mesenchymal Transition and Th2-Type Response in Patients With Chronic Rhinosinusitis With Nasal Polyps. 吸烟可增强慢性鼻窦炎合并鼻息肉患者的上皮-间质转化和th2型反应。
IF 6 4区 医学
Immune Network Pub Date : 2022-06-15 eCollection Date: 2022-08-01 DOI: 10.4110/in.2022.22.e35
Ki-Il Lee, Younghwan Han, Jae-Sung Ryu, Seung Min In, Jong-Yeup Kim, Joong Su Park, Jong-Seok Kim, Juhye Kim, Jubin Youn, Seok-Rae Park
{"title":"Tobacco Smoking Could Accentuate Epithelial-Mesenchymal Transition and Th2-Type Response in Patients With Chronic Rhinosinusitis With Nasal Polyps.","authors":"Ki-Il Lee,&nbsp;Younghwan Han,&nbsp;Jae-Sung Ryu,&nbsp;Seung Min In,&nbsp;Jong-Yeup Kim,&nbsp;Joong Su Park,&nbsp;Jong-Seok Kim,&nbsp;Juhye Kim,&nbsp;Jubin Youn,&nbsp;Seok-Rae Park","doi":"10.4110/in.2022.22.e35","DOIUrl":"https://doi.org/10.4110/in.2022.22.e35","url":null,"abstract":"<p><p>Tobacco smoking (TS) has been known as one of the most potent risk factors for airway inflammatory diseases. However, there has been a paucity of information regarding the immunologic alteration mediated by TS in patients with chronic rhinosinusitis with nasal polyps (CRSwNP). To identify the effect of TS, we harvested human tissue samples (never smoker: n=41, current smoker: n=22, quitter: n=23) and analyzed the expression of epithelial-derived cytokines (EDCs) such as IL-25, IL-33, and thymic stromal lymphopoietin. The expressions of Th2 cytokines and total serum IgE showed a type-2 inflammatory alteration by TS. In addition, the epithelial marker E-cadherin and epithelial-mesenchymal transition (EMT)-associated markers (N-cadherin, α-SMA, and vimentin) were evaluated. Histological analysis showed that EDC expressions were upregulated in the current smoker group and downregulated in the quitter group. These expression patterns were consistent with mRNA and protein expression levels. We also found that the local Th2 cytokine expression and IgE class switching, as well as serum IgE levels, were elevated in the current smoker group and showed normal levels in the quitter group. Furthermore, the expressions of E-cadherin decreased while those of N-cadherin, α-SMA, and vimentin increased in the current smoker group compared those in the never smoker group. Taken together, these results indicate that TS contributes to the deterioration of pathogenesis by releasing local EDCs and Th2 cytokines, resulting in EMT in patients with CRSwNP. We verified that alterations of immunological response by TS in sinonasal epithelium can play a vital role in leading to CRSwNP.</p>","PeriodicalId":13307,"journal":{"name":"Immune Network","volume":"22 4","pages":"e35"},"PeriodicalIF":6.0,"publicationDate":"2022-06-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/4f/8e/in-22-e35.PMC9433194.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"33453823","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 2
SOCS3 Attenuates Dexamethasone-Induced M2 Polarization by Down-Regulation of GILZ via ROS- and p38 MAPK-Dependent Pathways. SOCS3通过ROS-和p38 mapk依赖通路下调GILZ,减弱地塞米松诱导的M2极化。
IF 6 4区 医学
Immune Network Pub Date : 2022-06-13 eCollection Date: 2022-08-01 DOI: 10.4110/in.2022.22.e33
Hana Jeong, Hyeyoung Yoon, Yerin Lee, Jun Tae Kim, Moses Yang, Gayoung Kim, Bom Jung, Seok Hee Park, Choong-Eun Lee
{"title":"SOCS3 Attenuates Dexamethasone-Induced M2 Polarization by Down-Regulation of GILZ via ROS- and p38 MAPK-Dependent Pathways.","authors":"Hana Jeong,&nbsp;Hyeyoung Yoon,&nbsp;Yerin Lee,&nbsp;Jun Tae Kim,&nbsp;Moses Yang,&nbsp;Gayoung Kim,&nbsp;Bom Jung,&nbsp;Seok Hee Park,&nbsp;Choong-Eun Lee","doi":"10.4110/in.2022.22.e33","DOIUrl":"https://doi.org/10.4110/in.2022.22.e33","url":null,"abstract":"<p><p>Suppressors of cytokine signaling (SOCS) have emerged as potential regulators of macrophage function. We have investigated mechanisms of SOCS3 action on type 2 macrophage (M2) differentiation induced by glucocorticoid using human monocytic cell lines and mouse bone marrow-derived macrophages. Treatment of THP1 monocytic cells with dexamethasone (Dex) induced ROS generation and M2 polarization promoting IL-10 and TGF-β production, while suppressing IL-1β, TNF-α and IL-6 production. SOCS3 over-expression reduced, whereas SOCS3 ablation enhanced IL-10 and TGF-β induction with concomitant regulation of ROS. As a mediator of M2 differentiation, glucocorticoid-induced leucine zipper (GILZ) was down-regulated by SOCS3 and up-regulated by shSOCS3. The induction of GILZ and IL-10 by Dex was dependent on ROS and p38 MAPK activity. Importantly, GILZ ablation led to the inhibition of ROS generation and anti-inflammatory cytokine induction by Dex. Moreover, GILZ knock-down negated the up-regulation of IL-10 production induced by shSOCS3 transduction. Our data suggest that SOCS3 targets ROS- and p38-dependent GILZ expression to suppress Dex-induced M2 polarization.</p>","PeriodicalId":13307,"journal":{"name":"Immune Network","volume":"22 4","pages":"e33"},"PeriodicalIF":6.0,"publicationDate":"2022-06-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/d8/c3/in-22-e33.PMC9433193.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"33454302","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 4
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